THE 1.8 million Aussies with bad backs are more likely to have psychological distress and mental disorders.

The figures were revealed by the Australian Institute of Health and Welfare (AIHW) in a web-based snapshot of back problems.

One in 11 Australians, or 1.8 million people, had back problems in 2007-08 and were 2.5 times more likely to experience affective disorders such as depression, the data showed.

People with back problems were 1.8 times more likely to report an anxiety disorder and 1.3 times as likely to report a substance use disorder as people without back problems, AIHW spokeswoman Louise York said.

"They are also likely to report high or very high levels of psychological distress and more likely to report their health status as fair or poor," Ms York said.

Those with back problems were 3.4 times as likely to report some form of limitation in basic activities including dressing or going to the toilet and mobility, including getting in or out of bed, on a daily basis.

"Out of the 44 per cent of people with back problems who also reported activity limitations, about two-thirds reported mild to moderate core limitations, about one-third reported severe or profound activity limitations," Ms York said.

Aboriginal and Torres Strait Islanders were 25 per cent more likely to report having back problems than non-Indigenous Australians in 2004-05.

The snapshot said back problems had a considerable impact on both the sufferer and the community, with people aged 15 to 64 less likely to be employed full-time than people without back problems and 1.3 time more likely not to be in the labour force.

In 2009, 80 per cent of people with back problems had employment restrictions, were 1.1 times more likely to be restricted in the hours of work they could do and of those 36 per cent were permanently unable to work.

LEADING urologists have rejected claims that commercial interests are influencing the management of prostate cancer and say that over-treatment causing impotence and incontinence is being minimised.

On Tuesday, Melbourne cancer specialist Ian Haines said prostate cancer treatment had been hijacked by commercial interests, causing many men to be ''over-diagnosed'' with low-risk disease that led them to have damaging surgery unnecessarily.

An Associate Professor of Medicine from Monash University, he said PSA (prostate specific antigen) tests and Gleason scores to diagnose and score prostate cancers were unreliable and he criticised the marketing of expensive robotic surgery, saying it was only marginally better than standard prostatectomy procedures.

Professor Tony Costello - the Melbourne urologist who pioneered robotic surgery for prostate cancer - yesterday described his comments as ''provocative'' and stood by prostate cancer tests for many men and robotic surgery for prostate removal.

He said while hospitals had to ''claw back'' the millions of dollars invested in robotic surgical equipment, in his experience, it did not influence surgeons' advice to patients.

Furthermore, he said while no data had been published yet, he had found robotic surgery to be better for his patients, reducing rates of impotence and incontinence two years after surgery.

Professor Costello said growing evidence of over-treatment had caused a shift to more surveillance and less treatment for men with low-risk cancers. He said a registry set up to track cancers in Victoria showed about half of the 5500 men diagnosed in Victoria last year were being monitored to see if the cancer got worse. This showed urologists were acting in their patients' best interests, he said. ''If you get a positive biopsy for prostate cancer in Victoria, 46 per cent are getting surveillance … and you're more likely to be put on surveillance in private practice than you are in the public system, so there's no commercial advantage,'' he said.

Monash Medical Centre urologist and a spokesman for the Urological Society of Australia and New Zealand, Associate Professor Mark Frydenberg, said Gleason scoring was a reliable way to differentiate low, intermediate and high-risk cancers, allowing some men to have life-saving treatment. However, he said men deciding on treatment should seek various opinions because robotic surgery only offered marginal benefits. ''The differences to date are not huge. The complication rates for continence and potency appear similar,'' he said.

Several men contacted The Age yesterday with stories about prostate testing and treatment, including one man who was told he did not have cancer after having his prostate removed.

Urologists described his experience as very rare but acknowledged Gleason scoring — the system used by pathologists to label the aggressiveness of prostate cancers after microscopic examination of prostate tissue — was not always accurate.

A visiting US expert who is speaking at the Australasian Prostate Cancer Conference in Melbourne said although he felt confident recommending treatment for men who have a Gleason score of 7 and above on biopsy, Gleason scores often changed between biopsies before surgery and on pathological examination of the prostate after surgery.

‘‘About a third of the time it goes up, about a third of the time it goes down and about a third of the time it stays the same,’’ said Dr David Penson, the director of Surgical Quality and Outcomes Research at Vanderbilt University Medical Center in the US.

HealthDay News -- For older adults at risk of falls, integrating balance and strength training into routine daily activities may help reduce the rate of falls, according to a recent study.

Researchers examined whether a lifestyle-integrated approach to balance and strength training would reduce the rate of falls for older, high-risk individuals living at home. Participants (aged 70 years or older) were assigned to either a lifestyle-integrated functional exercise (LiFE) approach (107 participants); a structured program of exercise (105 participants); or a sham control program comprising gentle exercise (105 participants). Participants were assessed at baseline and after six and 12 months.

After 12 months, researchers identified 172 falls in the LiFE group, 193 in the structured-exercise group, and 224 in the control group, for an overall incidence of 1.66, 1.90, and 2.28 falls per-person, respectively. The rate of falls was reduced by 31% in the LiFE program vs. controls, while the difference between the LiFE group and the structured-exercise group was not significant. Compared with controls, participants in the LiFE group had significantly better static balance on an eight-level hierarchical scale, ankle strength, function, and participation. For dynamic balance there was a significant and moderate improvement in the LiFE and structured-exercise groups, respectively, compared with controls.

"The LiFE program provides an additional choice to traditional exercise and another fall prevention program that could work for some people," the authors write.

FRIDAY, Aug. 10 (HealthDay News) -- People who take a low-dose aspirin daily may not only be helping their hearts, but also reducing their odds of dying from cancer, according to American Cancer Society researchers.

The lower risk of dying from cancer associated with aspirin, however, may not be as great as previously thought, say the authors of the large new study.

And aspirin's possible side effects -- notably the higher risk of bleeding episodes -- need to be taken into account when considering its use, they added.

"Expert committees that develop clinical guidelines will consider the totality of evidence about aspirin's risks and benefits when guidelines for aspirin use are next updated," said lead researcher Eric Jacobs, the society's strategic director of pharmacoepidemiology.

Jacobs said, until there are new guidelines, he doesn't recommend taking aspirin for cancer prevention.

"Although recent evidence about aspirin use and cancer is encouraging, it is still premature to recommend people start taking aspirin specifically to prevent cancer," he said.

"Decisions about aspirin use should be made by balancing the risks against the benefits in the context of each individual's medical history. Any decision about daily aspirin use should be made only in consultation with a health care professional," he added.

The study was published in the Aug. 10 online issue of the Journal of the National Cancer Institute.

To look at the potential effect of daily aspirin use on cancer deaths, Jacobs' team used data from the Cancer Prevention Study II Nutrition Cohort, part of a larger long-term study on the effects of lifestyle factors on mortality.

This study included more than 100,000 men and women without a history of cancer, some of whom were taking aspirin daily.

Of the study participants, 5,138 eventually died from cancer.

Aspirin use was associated with an up to 16 percent lower risk of dying from cancer, which, however, was less than seen in another recent study, the researchers noted. In that analysis of randomized trials (where people were randomly assigned to either take aspirin or not take aspirin), aspirin use reduced cancer deaths by 37 percent during five years of follow-up and 15 percent during 10 years of follow-up, the authors noted in the report.

Nevertheless, "even a relatively modest benefit with respect to overall cancer mortality could still meaningfully influence the balances of risk and benefits of prophylactic [preventative] aspirin use," Jacobs' team concluded.

A limitation of the study is that it was an observational study, not a randomized trial. This could mean that the reduction in cancer deaths tied to aspirin use may be over- or under-estimated, the researchers noted.

Dr. John Baron, a professor of medicine at the University of North Carolina at Chapel Hill School of Medicine, who authored an accompanying journal editorial, said, "It's a remarkable idea that something that's in medicine cabinets around the world, and has been around for more than a century, can prevent cancer."

However, Baron is not recommending that people start taking aspirin to cut their odds for malignancy.

Why it works against cancer isn't known, Baron said, and he noted that the effect of aspirin is seen over time. For example, aspirin might start preventing colon cancer after a person had taken it for about 10 years.

During that time, however, that person might have gastrointestinal or brain bleeding caused by aspirin. So those risks and benefits need to be balanced, he noted.

The question is no longer whether aspirin prevents cancer, according to Baron, but rather whether the risks associated with aspirin are overshadowed by its benefits, he suggested. "But even the most pessimistic study shows a meaningful reduction," he added.

But while the new study found an association between aspirin use and reduced cancer risk, because it is not a randomized, controlled trial -- the "gold standard" for research -- it did not prove a cause-and-effect relationship.

Two studies suggest that two peptide agents used either together or individually with a low-dose of a standard chemotherapy drug might offer more effective cancer therapy than current standard single-drug treatments.

The studies used animal models of breast cancer to show that the peptide combinations dramatically delay tumor onset and progression by both inhibiting tumor growth and blocking the formation of new tumor blood vessels, say the researchers at the Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James) who conducted the study. In addition, the treatments caused few side effects.

The findings are described in two papers published online in the journal OncoImmunology. The first paper describes how vaccination with a HER2 peptide followed by treatment with a VEGF peptide inhibitor prevents tumor formation in a transplantable mammary tumor model. The second paper documents how either HER2 peptide or VEGF peptide treatment combined with low-dose paclitaxel effectively kills tumor cells in both the transplantable tumor model and a transgenic mammary tumor model.

"For treating cancer, combination therapies are much more effective than individual therapies, and peptides in combination, whether by vaccination or as therapy, appear to be safer, nontoxic, and taking us closer to a cure," says principle investigator Dr. Pravin Kaumaya, director of the division of vaccine development at the OSUCCC - James.

Kaumaya, who is a professor of obstetrics and gynecology, of molecular and cellular biochemistry, and of microbiology at Ohio State, led the research that developed the peptide agents. Peptides are short chains of amino acids, and the HER2 peptide and VEGF peptide are short amino-acid chains that mimic full-length HER2 and VEGF molecules.

The HER2 receptor molecule is important for controlling tumor growth in many cancers; the VEGF receptor molecule controls the formation of new blood vessels needed to feed tumors. Both molecules are overexpressed in many cancers.

In the new studies, the researchers investigated whether the peptide vaccine and the peptide inhibitor worked more effectively in combination, and also whether they could synergize with a standard chemotherapy agent, paclitaxel.

The HER2 peptide vaccine is injected into the body where it causes the immune system to generate antibodies to the HER2 receptor. These antibodies then bind to the overexpressed HER2 receptors on cancer cells, preventing them from stimulating tumor-cell proliferation. The VEGF therapeutic peptide binds directly to the VEGF receptor molecule, preventing it from directing the formation of new blood vessels.

In the first paper, the team shows that vaccinating mice with the HER2 peptide before aggressive mammary cancer cells are transplanted into the mice can delay the onset of the tumors. When this vaccination treatment was combined with weekly treatments of the VEGF peptide, tumor growth was significantly delayed. In animals given the VEGF peptide, which is engineered not to break down in the body, 40 percent of the animals did not develop tumors at all by the end of the experiment.

An online support site has been launched to help GPs caring for patients with chronic diseases such as diabetes. Chronic Disease Management-Net (cdmNet), enables patients, GPs and allied healthcare professionals to develop care plans, share medical histories, test results, updates on patients’ conditions, send referrals, and set appointment reminders, says Professor Leon Piterman of Monash University. “What cdmNet has done is provide an efficient clinical information system that makes health records available and accessible electronically,” Professor Piterman said. “This supports the GP’s decision making. It also provides a delivery system for information sharing and feedback with the care team. It ensures the team is working cohesively.” More than 10,000 chronic care patients, 1000 GPs and 3000 allied health practitioners who have...

CHILDREN with a severe brain disorder are being denied subsidies for a highly effective medication because the government insists they first try a riskier drug, say specialists who refuse to prescribe what they say is an outdated treatment.

Chris Seton,a paediatrician at the Children's Hospital at Westmead, said children with narcolepsy - a condition that causes them to fall asleep without warning, gives sudden bouts of muscle weakness and makes concentration difficult - could suffer life-threatening side effects, including psychosis, high blood pressure and heart palpitations, if they took the drug, dexamphetamine.

The stimulant is the only therapy routinely subsidised for the condition through the Pharmaceutical Benefits Scheme.

''I will not risk a child suffering the potential side effects,'' Dr Seton said. ''Faced with a choice between the two drugs to treat narcolepsy, nobody on the planet would chose the amphetamine.''

Dr Seton said he once admitted a 13-year-old girl to hospital suffering psychosis after she took dexamphetamine before the new drug - modafinil - became available in 2002.

None of the 35 children he was treating for narcolepsy had been able to access modafinil at the subsidised rate because he and his colleagues refused to prescribe the cheaper amphetamines, Dr Seton said.

But subsidy rules require children and adults to first try dexamphetamine and be taken off it because of side effects or lack of response before becoming eligible for modafinil.

Dr Seton said the effects of taking dexamphetamine long-term were unknown but people with narcolepsy were likely to need medication for the rest of their lives. Only about 200 Australian children suffered narcolepsy, meaning the total cost to government would be trivial.

Based on the standard dose, the national bill would be about $700,000 a year.

One of Dr Seton's patients, Harrison White, 6, began using modafinil two months ago and his condition improved ''almost immediately'' his mother, Tracy White, said.

''He used to wake up and have so much energy, then crash and fall asleep by 9am,'' Mrs White, of Wattle Grove, said. ''He had no sense of danger and would run out onto roads, climb things and try to jump off.

''Now he can play with his siblings like a normal little boy and chaos no longer dictates our lives.''

The medication costs Mrs White $170 a month, which will increase as Harrison approaches the standard dose. The financial impact was particularly hard because Harrison needed frequent other treatments. She said previous appeals to the government to make the drug more accessible had failed.

''My husband is overseas with the navy working full-time, so we can continue to provide for Harrison and our other three children,'' Mrs White said.

''I will not force Harrison to take dexamphetamine just so he can become eligible for a drug that is working.''

A spokeswoman for the Department of Health and Ageing said the Pharmaceutical Benefits Advisory Committee accepted applications and supporting evidence to amend drug listings.

On the snow-clotted plains of central Sweden where Wotan and Thor, the clamorous gods of magic and death, once held sway, a young, self-deprecating gene therapist has invented a virus that eliminates the type of cancer that killed Steve Jobs.

'Not "eliminates"! Not "invented", no!' interrupts Professor Magnus Essand, panicked, when I Skype him to ask about this explosive achievement.

'Our results are only in the lab so far, not in humans, and many treatments that work in the lab can turn out to be not so effective in humans. However, adenovirus serotype 5 is a common virus in which we have achieved transcriptional targeting by replacing an endogenous viral promoter sequence by…'

It sounds too kindly of the gods to be true: a virus that eats cancer.

Cheap to produce, the virus is exquisitely precise, with only mild, flu-like side-effects in humans. Photographs in research reports show tumours in test mice melting away.

'It is amazing,' Prof Essand gleams in wonder. 'It's better than anything else. Tumour cell lines that are resistant to every other drug, it kills them in these animals.'

Yet as things stand, Ad5[CgA-E1A-miR122]PTD – to give it the full gush of its most up-to-date scientific name – is never going to be tested to see if it might also save humans. Since 2010 it has been kept in a bedsit-sized mini freezer in a busy lobby outside Prof Essand's office, gathering frost. ('Would you like to see?' He raises his laptop computer and turns, so its camera picks out a table-top Electrolux next to the lab's main corridor.)

Two hundred metres away is the Uppsala University Hospital, a European Centre of Excellence in Neuroendocrine Tumours. Patients fly in from all over the world to be seen here, especially from America, where treatment for certain types of cancer lags five years behind Europe. Yet even when these sufferers have nothing else to hope for, have only months left to live, wave platinum credit cards and are prepared to sign papers agreeing to try anything, to hell with the side-effects, the oncologists are not permitted – would find themselves behind bars if they tried – to race down the corridors and snatch the solution out of Prof Essand's freezer.

I found out about Prof Magnus Essand by stalking him. Two and a half years ago the friend who edits all my work – the biographer and genius transformer of rotten sentences and misdirected ideas, Dido Davies – was diagnosed with neuroendocrine tumours, the exact type of cancer that Steve Jobs had. Every three weeks she would emerge from the hospital after eight hours of chemotherapy infusion, as pale as ice but nevertheless chortling and optimistic, whereas I (having spent the day battling Dido's brutal edits to my work, among drip tubes) would stumble back home, crack open whisky and cigarettes, and slump by the computer. Although chemotherapy shrank the tumour, it did not cure it. There had to be something better.

It was on one of those evenings that I came across a blog about a quack in Mexico who had an idea about using sub-molecular particles – nanotechnology. Quacks provide a very useful service to medical tyros such as myself, because they read all the best journals the day they appear and by the end of the week have turned the results into potions and tinctures. It's like Tommy Lee Jones in Men in Black reading the National Enquirer to find out what aliens are up to, because that's the only paper trashy enough to print the truth. Keep an eye on what the quacks are saying, and you have an idea of what might be promising at the Wild West frontier of medicine. This particular quack was in prison awaiting trial for the manslaughter (by quackery) of one of his patients, but his nanotechnology website led, via a chain of links, to a YouTube lecture about an astounding new therapy for neuroendocrine cancer based on pig microbes, which is currently being put through a variety of clinical trials in America.

I stopped the video and took a snapshot of the poster behind the lecturer's podium listing useful research company addresses; on the website of one of these organisations was a reference to a scholarly article that, when I checked through the footnotes, led, via a doctoral thesis, to a Skype address – which I dialled.

'Hey! Hey!' Prof Magnus Essand answered.

To geneticists, the science makes perfect sense. It is a fact of human biology that healthy cells are programmed to die when they become infected by a virus, because this prevents the virus spreading to other parts of the body. But a cancerous cell is immortal; through its mutations it has somehow managed to turn off the bits of its genetic programme that enforce cell suicide. This means that, if a suitable virus infects a cancer cell, it could continue to replicate inside it uncontrollably, and causes the cell to 'lyse' – or, in non-technical language, tear apart. The progeny viruses then spread to cancer cells nearby and repeat the process. A virus becomes, in effect, a cancer of cancer. In Prof Essand's laboratory studies his virus surges through the bloodstreams of test animals, rupturing cancerous cells with Viking rapacity.

The Uppsala virus isn't unique. Since the 1880s, doctors have known that viral infections can cause dramatic reductions in tumours. In 1890 an Italian clinician discovered that prostitutes with cervical cancer went into remission when they were vaccinated against rabies, and for several years he wandered the Tuscan countryside injecting women with dog saliva. In another, 20th-century, case, a 14-year-old boy with lymphatic leukaemia caught chickenpox: within a few days his grotesquely enlarged liver and spleen had returned to ordinary size; his explosive white blood cell count had shrunk nearly 50-fold, back to normal.

But it wasn't until the 1990s, and the boom in understanding of genetics, that scientists finally learnt how to harness and enhance this effect. Two decades later, the first results are starting to be discussed in cancer journals.

So why is Magnus – did he mind if I called him 'Magnus'? – about to stop his work?

A reticent, gently doleful-looking man, he has a Swedish chirrup that makes him sound jolly whatever his actual mood. On the web, the first links to him proclaim the Essand Band, his rock group. 'Money,' he said. 'Lack of.'

'Lack of how much money? Give me a figure,' I pressed. 'What sort of price are we talking about to get this virus out of your freezer and give these people a chance of life?'

Magnus has light brown hair that, like his voice, refuses to cooperate. No matter how much he ruffles it, it looks politely combed. He wriggled his fingers through it now, raised his eyes and squinted in calculation, then looked back into his laptop camera. 'About a million pounds?'

More people have full-blown neuroendocrine tumours (known as NETs or carcinoids) than stomach, pancreas, oesophagus or liver cancer. And the incidence is growing: there has been a five-fold increase in the number of people diagnosed in the last 30 years.

In medical school, students are taught 'when you hear hoof beats, think horses not zebras' – don't diagnose a rare disease when there's a more prob-able explanation. It leads to frequent misdiagnoses: until the death of Steve Jobs, NETs were considered the zebras of cancer, and dismissed as irritable bowel syndrome, flu or the patient getting in a tizz. But doctors are now realising that NETs are much more prevalent than previously thought. In a recent set of post-mortem investigations, scientists cut open more than 30,000 bodies, and ran their hands down the intestines of the dead as if they were squeezing out sausage skins. One in every 100 of them had the distinctive gritty bumps of NETs. That's two people in every rush-hour tube carriage on your way home from work, or scaled up, 700,000 people in Britain, or roughly twice the population of the city of Manchester. The majority of these tumours are benign; but a small percentage of them, for reasons that no one understands, burst into malignancy.

Many other cancers, if they spread, acquire certain features of neuroendocrine tumours. The first person to own a successful anti-neuroendocrine cancer drug – it doesn't even have to cure the disease, just slow its progress as anti-retrovirals have done with Aids – will be not only healthy but also Steve Jobs-rich. Last year the pharmaceuticals giant Amgen bought a cancer-assassinating version of the herpes virus for $1 billion. That Magnus's virus could be held up by a minuscule £1 million dumbfounded me.

'That's a banker's bonus,' I said. 'Less than a rock star's gold toilet seat. It's the best bargain going. If I found someone to give you this money, would you start the clinical trials?'

'Of course,' replied Magnus. 'Shall I ask the Swedish Cancer Board how soon we can begin?'

I do not have a million pounds. But for £68 I flew to Uppsala. I wanted to pester Prof Essand about his work, face to face, and see this virus, face to petri dish. I wanted to slip some into my mittens, smuggle it back to England in an ice pack and jab it into Dido.

Magnus's work is already funded by the Swedish Cancer Society and the Swedish Children Cancer Society (neuroblastoma, the most common cancer in infants, is a type of neuroendocrine tumour). A virus that he previously developed (against prostate cancer) is about to enter human trials in Rotterdam, supported by a European Union grant.

The difficulty with Magnus's virus is not that it is outré, but that it is not outré enough. It is a modified version of an adenovirus, which is known to be safe in humans. It originates from humans, occurring naturally in the adenoids. The disadvantage is that it is too safe: the immune system has had thousands of years to learn how to dispatch such viruses the moment they stray out of the adenoids. It is not the fact that Magnus is using a virus to deal with cancer that makes his investigation potentially so valuable, but the novel way he has devised to get round this problem of instant elimination by the immune system, and enable the virus to spread through tumours in other parts of the body.

The closer you get to manipulating the cellular forces of human existence, the more you sound like a schoolboy babbling about his model aeroplane. Everything in the modern genetics lab is done with kits. There are no fizzing computer lights or fractionating columns dribbling out coagulations of genetic soup in Magnus's lab; not a single Bunsen burner. Each narrow laboratory room has pale, uncluttered melamine worktops running down both sides, wall units above and small blue cardboard cartons dotted everywhere. Even in their genetics labs, Swedes enjoy an air of flatpack-ness. The most advanced medical lab in the world, and it looks like a half-fitted kitchen.

To make and test their virus, Magnus buys cell lines pre-fab (including 'human foreskin fibro-blast') for $50-100 from a company in California; DNA and 'enzyme mix' arrive in $179 packets from Indiana; protein concentrations are tested 'according to the manufacturer's instructions' with a DIY kit ($117) from Illinois; and for $79, a parcel from Santa Cruz contains (I haven't made this up) 'horseradish peroxidase conjugated donkey anti-goat antibody'.

In a room next to Magnus's office, a chatty woman with a ponytail is putting DNA inside bacteria. This God-like operation of primal delicacy involves taking a test tube with a yellow top from a $146 Qiagen kit, squirting in a bit of liquid with a pipette and putting the result in a box similar to a microwave: 'turn the dial to 25 kilovolts and oophlah! The bacteria, they get scared, they let the DNA in. All done,' the woman says. As the bacteria divide, the desirable viral fragments increase.

What costs the £1 million (less than two per cent of the price of Francis Bacon's Triptych 1976) that Magnus needs to bring this medicine to patients is not the production, but the health-and-safety paperwork to get the trials started. Trials come in three phases. What Magnus was suggesting for his trifling £1 million (two Mont Blanc diamond-encrusted pens) was not just a phase I trial, but also a phase II, which, all being well, would bring the virus right to the point where a big pharmaceuticals company would pay 10 or 100 times as much to take it over and organise the phase III trial required by law to presage full-scale drug development.

'So, if Calvin Klein or Elton John or… Paris Hilton stumped up a million, could they have the virus named after them?'

'Why not?' Magnus nodded, showing me the bacteria incubator, which looks like an industrial clothes washer, only less complicated. 'We can make an even better one for two million.'

There are reasons to be cautious. A recent investigation by Amgen found that 47 of 53 papers (on all medical subjects, not just viruses) by academics in top peer-reviewed science journals contained results that couldn't be reproduced, even though company scientists repeated the experiments up to 50 times. 'That's why we have to have such a careful peer-review process,' Dr Tim Meyer, Dido's energetic, soft-spoken oncologist, warns. 'Everybody thinks that their new treatment for cancer is worth funding, but everybody is also keen that only good-quality research is funded.' Similar to Prof Essand in youth but less polite of hair, Dr Meyer is the co-director of the Experimental Cancer Medicine Centre at University College London. Beside his office, banks of white-coated researchers are bent over desks, busy with pipettes and microscopes. His team pursues an exciting brew of new anti-cancer ideas: antibody-targeted therapy, vascular therapy, DNA binding agents and photodynamic therapy. Each of these shows remarkable promise. But even for such a brilliant and innovative team as this, money is not flowing.

Everyone in cancer science is fighting for ever-decreasing small pools of cash, especially now the government has started tiptoeing into charities at night and rifling the collection boxes. It is big news that Dr Meyer and the UCL team won a grant of £2.5 million, spread out over the next five years, to continue his institute's cutting-edge investigations into cancers that kill off thousands of us every week: leukaemia; melanoma; gynaecological, gastrointestinal and prostate cancers. Without this money, he would have had to sack 13 members of staff. The sum of £2.5 million is roughly what Madonna earns in 10 days.

He peers at Magnus's pairs of photographs of splayed rodents with glowing tumours in one shot that have vanished in the next. He knows the Uppsala neuroendocrine team well and has great respect for them. 'It may be good,' he agrees. But until Magnus's findings are tested in a clinical trial, nobody knows how good the work is. Astonishing results in animals are often disappointing in humans. 'We all need to be subject to the same rules of competitive grant funding and peer review in order to use scarce resources in the most effective manner.'

Back at home with whisky and fags, I nursed my entrepreneurialism. There are currently about half a dozen cancer research institutes in Europe developing adenoviruses to treat cancer – all of them pathetically short of cash. Enter the Vanity Virus Initiative. Pop a couple of million over to Uppsala University, and you will go down in medical books as the kind heart who relieved Ad5[CgA-E1A-miR122]PTD of its hideous hump of a moniker, and gave it the glamour of your own name. What's the worst that can happen? Even if Magnus's innovations don't work in clinical trials the negative results will be invaluable for the next generation of viruses. For the rest of time, your name will pop up in the reference sections of medical papers as the (insert your name here) virus that enabled researchers to find the cure for cancer by avoiding Magnus's error.

On my third glass of whisky, I wrote an email to Dr Meyer suggesting that he issue a shopping list each year at the time that bankers receive their bonuses, which could be circulated in the City. The list would itemise the therapies that his Experimental Cancer Medicine Centre have selected for support, and quantify how much would be needed in each case to cover all outstanding funds and ensure that the work is branded with your name.

The corridors connecting the different research departments of the Uppsala medical campus are built underground, in order to protect the staff from death during the Swedish winters. Professors and lab technicians zip back and forth along these enormous rectangular tunnels on scooters, occasionally scratching their heads at the tangled intersections where three or four passageways meet at once, then pushing off again, gowns flying, one leg pounding the concrete floor like a piston, until they find the right door, drop the scooter and rise back upstairs by lift. Suspended from the ceiling of these corridors is a vacuum tube that schluuuuups up tissue samples at top speed, and delivers them to the appropriate investigative team. Magnus led me along these tunnels to the Uppsala University Hospital, to visit the chief oncologist, Kjell (pronounced 'Shell') Oberg – the man who will run the trial once the money is in place.

'The trouble with Magnus's virus is Magnus is Swedish,' he says, wincing and clutching the air with frustration.

'It is so,' Magnus agrees sorrowfully. Swedishly uninterested in profiteering, devoted only to the purity of science, Magnus and his co-workers on this virus have already published the details of their experiments in leading journals around the world, which means that the modified virus as it stands can no longer be patented. And without a patent to make the virus commercial, no one will invest. Even if I could raise the £2 million (I want only the best version) to get the therapy to the end of phase II trials, no organisation is going to step forward to run the phase III trial that is necessary to make the therapy public.

'Is that because pharmaceuticals companies are run by ruthless plutocrats who tuck into roast baby with cranberry sauce for lunch and laugh at the sick?' I ask sneerily.

'It is because,' Kjell corrects me, 'only if there's a big profit can such companies ensure that everyone involved earns enough to pay their mortgage.'

There is no ready source of public funds, either. For reasons understood only by Wotan and Thor, the Swedish government refuses to finance clinical trials in humans, even when the results could potentially slash the country's health bill by billions of kronor.

All is not lost, however. Kjell does not have to wait until the end of the trials – which could take as much as 10 years – for the full, three-phase process before being able to inject Magnus's virus into his patients, because as soon as the test samples are approved and ready for use, he can by European law start offering the medicine, on an individual basis, to patients who sign a waiver confirming that they're prepared to risk experimental treatments. Within 18 months he could be starting his human case-studies.

At several moments during my research into this cancer-delaying virus from the forests of Scandinavia I have felt as though there were someone schlocky from Hollywood operating behind the scenes. The serendipitous discovery of it on the internet; the appalling frustration of being able to see the new therapy, to stand with my hand against the freezer door knowing that it is three inches away, not well-guarded, and that it might work even in its crude current state, but that I may not use it; the thrill of Kjell Oberg's powerful support; the despair over the lack of such a silly, artificial thing as a patent. Now, Dr Leja steps into the narrative: she is the virologist whose brilliant doctoral thesis first put me on to the cancer-eating-virus-left-in-a-freezer, and whose name heads all the subsequent breakthrough research papers about this therapy. She turns out to be 29, to look like Scarlett Johansson and to wear voluptuous red lipstick.

Justyna Leja slinks up from her chair, shakes my hand and immediately sets off into a baffling technical discussion with Magnus about a good way to get the patent back for the virus, by a subtle manipulation that involves something called a 'new backbone'. She also has in mind a small extra tweak to the new-backboned microbe's outer coat, which will mean that the virus not only bursts the cancer cells it infects, but also provokes the immune system to attack tumours directly. It will be easy to see if it works in animals – but is it worth lumbering the current virus with it for use in humans, who tend to be less responsive? The extra preparatory work could delay the phase I and II trials for a further year.

Back at his lab, Magnus opened up the infamous freezer. I took a step towards the plastic flasks of virus: he nipped the door shut with an appreciative smile.

'What would you do,' I asked bitterly, returning my hand to my pocket, 'if it were your wife who had the disease, or one of your sons whose photograph I saw on your desk?'

He glanced back at the freezer. Although his lab samples are not made to pharmaceutical grade, they would be only marginally less trustworthy than a fully-sanctioned, health-and-safety certified product that is between 1,000 and 10,000 times more expensive.

'I don't know,' he groaned, tugging his hair in despair at the thought. 'I don't know.'

HEALTH Minister Jillian Skinner is prepared to push people out of hospital early to help achieve a $3 billion budget cut.

Explaining the government's cuts to the health portfolio yesterday, Ms Skinner said that "most of the money" saved would be through "better models of care, through, for example, not keeping patients in hospital as long as they should be".

What do you think of the cuts to the health portfolio? Leave a comment below

"I think a lot of people are very pleased not to be kept in hospital longer than they need to," Ms Skinner said.

"I have a brand new granddaughter. Her mother was in hospital for two nights, she spent the next two nights in a five-star hotel room. This is a private hospital, this is what they do now ... It's actually better for the mum ... and more efficient for the hospital to pay for a five-star hotel room than a $2000-$3000 acute bed."

Ms Skinner said her cuts would include "treating them in new ways in emergency departments, more outpatient services, less reliance on locums and other agency staff and ... restructuring the health system".

"Give you a simple example. When I was a kid I had my appendix out. I was in hospital for 10 days. Appendectomy now is keyhole surgery and frequently now it's a day only," she said.

Ms Skinner claimed that $2.2 billion of the $3 billion in cuts would be redirected to "frontline services" but her comments appeared to contradict the government line that money was being taken from the backroom and put on the frontline.

NSW AMA vice-president Dr Saxon Smith said decisions on when to release patients from hospital "need to be made on appropriate clinical grounds, not just to save money". He said it was only in very rare cases patients could be let out of hospital on the same day as having had an appendectomy.

Ms Skinner's comments are the latest gaffe by a minister after Education Minister Adrian Piccoli said he "slept well at night" over the $1.7 billion in education cuts and Transport Minister Gladys Berejiklian released a largely unfunded $137 billion transport master plan.

Treasurer Mike Baird said yesterday the cuts were necessary because the government had lost $10 billion in revenue - including $5.3 billion in GST revenue - over four years because of deteriorating confidence in the economy.

"From the day we came in to the last budget we lost $10 billion worth of (projected) revenue," Mr Baird said.

"There's still people in jobs, there's some economic growth but because there's been uncertainty (over property) ... share portfolios are down ... Lack of confidence means consumers are spending less and saving more.

"If you don't act now you'll play catch-up and South Australia and Queensland have both had their (credit) ratings downgraded."

Opposition Leader John Robertson accused Ms Skinner of being "out of touch".

"While I'm delighted her daughter-in-law had such a positive experience in a private hospital, most people simply can't afford to pay for a five-star hotel to recover from childbirth or surgery and they rely on the public hospital system to look after them," Mr Robertson said.

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